A Previously Healthy 37-Year-Old Man With Acute Hypoxic Respiratory Failure and Fevers

Abstract

A previously healthy 37-year-old man initially presented to a hospital near his home with persistent cough after failing outpatient azithromycin for empiric treatment of pneumonia. He was newly employed as a bulldozer operator burying trash in a landfill in Virginia, which he continued throughout his illness. He owned two healthy dogs, had never traveled outside the state, and denied a history of cigarette smoking, alcohol, and substance use. His WBC count was 13.4 × 10⁹/L (11% eosinophils). CT scan of the chest showed ground glass opacities. Subsequent bronchoscopy with BAL of the right middle lobe showed eosinophilic predominance (46%); transbronchial biopsy of right lower lobe was performed. Infectious and autoimmune work up that was negative included blood, urine, and BAL cultures, BAL Pneumocystis pneumonia direct immunofluorescence assay, urine legionella antigen, serum HIV antibody, antinuclear antibodies, anti-neutrophil cytoplasmic antibodies, and angiotensin converting enzyme. After improvement in hypoxia with inpatient corticosteroid therapy, he was discharged home with a two week course of prednisone for a presumptive diagnosis of acute eosinophilic pneumonia. He subsequently experienced worsening fever and difficulty breathing; six weeks after his symptoms began, he was admitted to our hospital.

Figure 1

Chest radiograph on admission.

Figure 2

Chest CT scan on admission shows bilateral consolidations (A, B, C) with cavitary lesions in the left lower lobe (B, C).

Figure 3

BAL direct microscopy stained with Gömöri methenamine silver demonstrated fungal septate hyphae with dichotomous branching.

Figure 4

Lung tissue from transbronchial biopsy demonstrated non-caseating granulomas (hematoxylin-eosin stain, 100X).

Figure 5

Flow cytometric histograms of oxidation of DHR 123 to the green fluorescent rhodamine 123. Neutrophils are exposed to PMA, which induces oxidative burst and the production of reactive oxygen intermediates (ROI). DHR is then introduced, which is converted to rhodamine only in the presence of ROI. Rhodamine has a similar spectral profile to FITC. An absence of fluorescence indicates an absence of ROI, and thus deficiency of NADPH oxidase. The y-axis is cell count and the x-axis is fluorescence intensity of rhodamine (FITC channel). A, Patient's unstimulated neutrophils. B, Patient's PMA-stimulated neutrophils show a broad and dim fluorescence consistent with residual reactive oxygen intermediate production. C, Normal control PMA-stimulated neutrophils show intense fluorescence. DHR = dihydrorhodamine; FITC = fluorescein isothiocyanate; PMA = phorbol myristate acetate.

Figure 6

CT scan of the head with multiple parenchymal hypodensities.